Chapter 6
Quantitative and Thought Questions
6.1 Little change in the resting membrane potential would occur when the pump first stops because the pump’s direct contribution to charge separation is very small. With time, however, the membrane potential would depolarize progressively toward zero because the Na 1 and K 1 concentration gradients, which depend on the Na 1 /K 1 -ATPase pumps and which give rise to the membrane potential, run down.
6.2 The resting potential would decrease (i.e., become less negative) because the concentration gradient causing net diffusion of this positively charged ion out of the cell would be smaller. The action potential would fire more easily (i.e., with smaller stimuli) because the resting potential would be closer to threshold. It would repolarize more slowly because repolarization depends on net K 1 diffusion from the cell, and the concentration gradient driving this diffusion is lower. Also, the after hyperpolarization would be smaller.
6.3 The hypothalamus was probably damaged. It plays a critical role in appetite, thirst, and sexual capacity.
6.4 The drug probably blocks cholinergic muscarinic receptors. These receptors on effector cells mediate the actions of parasympathetic nerves. Therefore, the drug would remove the slowing effect of these nerves on the heart, allowing the heart to speed up. Blocking their effect on the salivary glands would cause the dry mouth. We know that the drug is not blocking cholinergic nicotinic receptors because the skeletal muscles are not affected.
6.5 Because the membrane potential of the cells in question depolarizes (i.e., becomes less negative) when Cl 2 channels are blocked, we can assume there was net Cl 2 diffusion into the cells through these channels prior to treatment with the drug. Therefore, we can also predict that this passive inward movement was being exactly balanced by active transport of Cl 2 out of the cells.
6.6 Without acetylcholinesterase, more acetylcholine would remain bound to the receptors, and all the actions normally caused by acetylcholine would be accentuated. Consequently, there would be significant narrowing of the pupils, airway constriction, stomach cramping and diarrhea, sweating, salivation, slowing of the heart, and decrease in blood pressure. On the other hand, in skeletal muscles, which must repolarize after excitation in order to be excited again, there would be weakness, fatigue, and finally inability to contract. In fact, lethal poisoning by high doses of cholinesterase inhibitors occurs because of paralysis of the muscles involved in respiration. Low doses of these compounds are used therapeutically.
6.7 These K 1 channels, which open after a short delay following the initiation of an action potential, increase K 1 diffusion out of the cell, hastening repolarization. They also account for the increased K 1 permeability that causes the after hyperpolarization. Therefore, the action potential would be broader
(that is, longer in duration) and would return to resting level more slowly, and the after hyperpolarization would be absent.
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